Abstract
Nonalcoholic fatty liver disease (NAFLD) is common worldwide and closely associated with metabolic dysfunction. NAFLD leads to a higher risk of development of severe liver diseases, such as nonalcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma (HCC). To date, no pharmacotherapy targeting NAFLD has received general approval. Adlay is a plant that has been used as traditional herbal medicine in Asia and is a promising candidate to solve this global issue. We have established a mouse model of NAFLD by feeding a high-fat diet (HFD) for 10 weeks. Here, ethanolic or water extracts of adlay seed (ASE and ASW, respectively), mixed with HFD, were fed to the mice for 10 weeks. The ASE and ASW treatment ameliorated hyperglycemia and improved the glucose tolerance and insulin resistance in the HFD mice. Hyperlipidemia in HFD mice was prevented by the ASE and ASW diet. In addition, the ASE and ASW supplementation attenuated hepatic steatosis and inflammation, improved liver function, and caused no harm to the kidneys. Moreover, the mechanism of the effect of ASE and ASW on inhibiting hepatic lipogenesis and inducing fatty acid β-oxidation was certified by the simulated human fatty liver cell model. Our study showed the regulatory potential of the extracts of adlay seeds for alleviating NAFLD, as well as related liver and metabolic diseases.
Highlights
Hao Chiang,1 Hsu-Feng Lu,2,3 Jui-Chieh Chen,4 Yu-Hsin Chen,5 Hsi-Tai Sun,6 Hsiu-Chen Huang,7 Hsiao-Hsuan Tien,1 and Cheng Huang 1,8
Insulin resistance, resulting from long-term, sustained hyperglycemia, leading to impaired insulin-stimulated glucose utilization and glycogen synthesis, is the key pathogenic feature of metabolic syndrome and is Evidence-Based Complementary and Alternative Medicine regarded as the most common risk factor for the development and progression of nonalcoholic fatty liver disease (NAFLD) [7]. e pathophysiology of Nonalcoholic fatty liver disease (NAFLD) is induced by multiple factors [8], such as obesity, insulin resistance [9], and dysregulation of lipid metabolism [10], which interact with each other in a dynamic manner
To determine the effect of ASE and ASW on NAFLD, we used an established high-fat diet (HFD)-induced mouse model of NAFLD, produced by feeding an HFD, and the HFD mice were treated with ASE or ASW for 10 weeks (Figure 1(a)). e body weight gain and the adipose tissue weight of the HFD group were significantly greater than the ND group (Table 1). is suggests that the HFD mice had a tendency to develop metabolic complications, which fit the main characteristics of central obesity. e amount of food consumed by the mice did not differ significantly among the groups
Summary
E. TM ethanolic extract of adlay seeds (ASE; CoiXtreme , A.T.P. CO., LTD., Taiwan) was concentrated and particulated with lactose powder and using coixol as an indicator compound at a concentration of 620 ppm. E analysis of blood glucose, serum insulin, intraperitoneal glucose tolerance test, and the homeostasis model assessment of insulin resistance index were performed as described previously [19]. Erefore, serum TG, TC, HDLC, and LDLC levels were monitored to evaluate the effect of ASE and ASW on lipid metabolism. We found that feeding HFD for 10 weeks significantly increased the levels of serum TG, TC, and LDLC, leading mice to hyperlipidemia. E level of serum HDLC did not differ significantly from the HFD group after ASE or ASW treatment (Figure 2(c)). Asterisks indicate that the values differed significantly from the control (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; #p < 0.05; ##p < 0.01; and ###p < 0.001)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
